This review aims to investigate the potential mechanisms driving the transition from acute vestibular events to chronic dizziness, focusing on the roles of neural sensitization and psychological sensitization in symptom persistence. The evolution of vestibular dizziness is analyzed from the perspectives of vestibular compensation, sensory reweighting, and the fear-avoidance model. After acute vestibular injury, central nervous system function can be partially restored through vestibular compensation, sensory reweighting, and synaptic plasticity. However, this recovery process is often accompanied by increased visual dependence, which provides a foundation for the development of neural sensitization. The abnormal integration of proprioceptive and visual input described by the fear-avoidance model not only contributes to central sensitization but also reveals the core feature of psychological sensitization: perceptual amplification driven by catastrophizing cognition and avoidance behavior. Patients with chronic dizziness exhibit hypersensitivity to visual and proprioceptive stimuli and reduced sensory processing thresholds, which reflects abnormal sensory gain at the level of neural sensitization. Psychological factors, in turn, maintain or exacerbate neural sensitization by modulating proprioceptive processing and limbic system activity. Neural sensitization and psychological sensitization mutually reinforce each other, constituting a critical link in the transition from acute vestibular events to chronic dizziness. Comprehensive interventions targeting sensory reweighting, fear-avoidance behavior, and psychiatric comorbidity may help interrupt this process.
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Wang et al. (2026) studied this question.
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